We use conventional criteria and look for the change in FEV 1. Would you consider that a reasonable thing to do, or are we unduly putting the patients at risk? There's a third signal that we use. We call it sustained chest tightness. This refers to the patient's report of progressive chest tightness lasting at least 2 minutes, sometimes combined with auscultation by the therapist to determine that air flow is reduced. That assures that at least one threshold airway measurement is exceeded, but that we don't ignore clinical evidence of sustained and progressive patient distress.
This has improved test accuracy, but also recognizes the subject's safety. We do the same thing. If we get to 8 mg and they're coughing or have tightness, even though they haven't reached FEV 1 criteria, but they've reach conductance criteria by that point, I stop the test.
To go back to your first slide, I don't think what you presented was atypical. I'm not a pulmonary physiologist, but many times I'll have people coming in who complain of shortness of breath and use medications without relief. I'll begin the measurement of R aw , and they are abnormal even though lung functions tend to be really quite normal. We began our discussion this morning talking about phenotypes, and asthma is a very broad definition and it may not encompass all things that have altered physiology.
And we don't have good data, necessarily, on people who have just increases in R aw. We don't test them under various conditions, nor do we necessarily test them after we've given them medications like inhaled corticosteroids.
This is certainly not the usual approach to patients who come in with symptoms compatible with asthma. In patients who have symptoms of asthma but largely normal lung function, vocal cord dysfunction is a high probability. These individuals have an inspiratory loop cutoff. Addressing these patients requires going through an appropriate differential diagnosis and matching the lung function abnormalities to the clinical picture.
I would agree with you, but in this case the symptoms were very responsive to the inhaler, and I don't know if that was a placebo effect or real. But we did document physiology that at least helps us understand and be convinced that the medicine is doing some good.
I will say there's a decent literature from the s and s looking at this different response to bronchodilator and bronchoconstrictor in the central airways versus peripheral airways. Nobody knows quite what to make of that, and it's a hot topic now because we're all interested in giving these small particle HFA [hydrofluoroalkane] solution steroids that penetrate deeper, but we don't know the ultimate clinical effect.
I think there is something phenotypically different between asthmatics in particular who have disease location in different parts of their lung. Like you say, we just don't understand a lot about it yet. Right, we don't know what part of the tree they're on: the beginning part of the tree or somewhere else. It's amazing how long these things have been around and how little sophistication we have in knowing what to do with the data.
When I finished my training, I thought I knew what cystic fibrosis was, and I thought I knew what asthma was. And now I'm looking at retirement, with cystic fibrosis being defined with a range between sterility in males with no lung disease and no gastrointestinal disease and the full-blown syndrome with severe bronchiectasis and malnutrition.
We still know it's all related to the same protein, but variations in expression and type of the defect change the presentation dramatically. I think asthma has become way more complicated. The lung has very few tricks up its sleeve, and reversible bronchospasm is one of those tricks.
Hence, reversible bronchospasm may have manifestations that we may later come to understand as several different disease processes. Hence, I'm not surprised that we keep seeing very different types of expressions of asthma while we actually may be looking at different diseases that we just haven't sorted out yet.
I agree, and that's why some are calling asthma a syndrome as opposed to a disease: because it encompasses facets of different types of symptoms, airway dysfunction, inflammation, and so on. You mentioned you measure R aw as well as FEV 1 during methacholine challenges. Do you do that all the time? We do exercise challenge with the treadmill, and we only do spirometry during that challenge. It's physically located in a different room than the body box, and the rooms are always going concurrently, so it makes it hard to do.
Now, have you found that you see the changes in the R aw before you see changes in the FEV 1? If I can take the discussion into the ICU just for a few minutes, which I guess is fair because I heard you say you just came off service in the unit. Is that a worthwhile thing to do? Do you do that in your practice? We can't take the body box into the ICU. The answer is yes, I think it is worthwhile, and we do that in our practice.
We don't follow R aw per se, but I look at the difference between peak and plateau pressure as a surrogate for respiratory system resistance. In obstructed patients this is also a valuable way to teach our fellows and residents. When we're giving bronchodilator therapy, one way we know the patient is getting better is their peak pressures are coming down, the difference in peak and plateau pressure is narrowing, and presumably the patient is moving better air.
But as we've been saying the whole conference, it's not just one factor: that's one of many we're looking at. Yes, I use that as part of the monitoring of these patients. When you said you use 2 of the 3 measures to stop the bronchoprovocation test, do you deem that positive then? I don't use 2 of our 3 specifically, like Bo [Pichurko], but for us the clinical impression still overrides everything. If the patient is coughing or tight, no matter what the values are, the technologist will try to get a body box measurement and spirometry at that point in time.
Then, if either criteria are met, FEV 1 or conductance, we will stop. If the patient is asymptomatic, we'll go up to 16 mg, and we still continue to look for both responses. One of my jobs as pulmonary-function-testing director is to be available if they have any questions, and it's not uncommon for me to run up to the lab and take a look at someone in the midst of their challenge to try and help the techs determine if it's safe to go on or not.
We try to put the clinical response to methacholine together with both aspects of physiology. Do you then take the response to albuterol the ability to quickly reverse the bronchospasm into account when interpreting the results?
I take it into consideration, but it's not the primary thing we look at. As I've said before, I've never seen a patient not reverse. Sometimes we have to give another 2 puffs. Typically we give 2, but sometimes it takes 4.
I'm not sure I was hearing the 2 of you correctly about this. You're saying that you stopped the test for safety reasons, even if you haven't dropped the FEV 1 , if you have symptoms, such as wheezing and coughing.
Are you saying you call the test positive with just subjective end points? No, I won't call the test positive with just subjective end points. Then, and I'm not fudging on this, I'll say this needs to be put into the clinical context. If that was my patient, it's still someone I might put on a 6-week trial of inhaled corticosteroids and see how they do. Similarly, I would require exceeding the diagnostic threshold for at least one of those objective measures before concluding the provocation study.
The additional support of patient symptomatology serves to validate the objective measure. Didn't we talk this morning about the idea that the methacholine challenge test was a good test to rule out asthma? So, within what you just said, how do we fit that? To me, a negative test is someone who goes up to 16 and flies through it, and there are no changes physiologically, and they have no discomfort.
I don't think they have asthma if they respond that way. Well, one could argue the other way. Allan, I think we've defined the positive response to methacholine for what we consider to be the classical, clinical asthma, haven't we? You wonder if we've been overly constrictive on what we're calling a positive test as far as the disease is concerned. Like you said, when I began work 35 years, ago I really felt like I knew a lot about asthma, and as time has gone on, my understanding of the ambiguities has increased.
I think we need to open things up a little bit and look at these various characterizations and responses to tests to give us some ideas about abnormalities in functions and what they really mean.
No disagreement about that, because I am coughing and wheezing even though my PC 20 is greater than We have these arbitrary cutoffs. This [showing an additional slide of a series of flow-volume loops during a methacholine challenge that illustrates progressive truncation of inspiratory flow] is a patient who responded to methacholine with vocal cord dysfunction. The FEV 1 didn't change a bit. The conductance did change, as you would imagine, because R aw elevated due to closure of the cords.
This is a nice example of someone who almost had no symptoms: she kind of got a little cough and a little discomfort. I think we have to take all the information together in making our clinical judgments. But if everything goes smoothly, at least at that point in time, I would consider it a negative challenge and I think it has a high specificity in that case. One last question. You're doing full FVC maneuvers then, during your methacholine challenge?
With R aw? Do you train these patients before you test them, for 6 weeks or so? It seems that this would be very fatiguing for the patient and quite time consuming.
With the Aridol bronchial challenge test, we used only FEV 1 maneuvers after the baseline spirometry FVC maneuver, and with the methacholine test we and others prefer the FEV 1 maneuver because of patient fatigue. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address. Skip to main content. Research Article Conference Proceedings. David A Kaminsky. Abstract Spirometry is considered the primary method to detect the air flow limitation associated with obstructive lung disease.
Introduction Spirometry is considered the gold standard method to measure air flow limitation. Physiology Resistance to air flow in the lung is determined by measuring the pressure difference across the airways and dividing this difference by the flow.
Clinical Utility of sR aw and sG aw Due to geometric considerations, whereby the total cross sectional area of the airways decreases dramatically as one moves from the periphery to the central regions of the lung, any measure of overall airway resistance, like sG aw , will be very sensitive to central airway pathology but less sensitive to peripheral changes.
Measurement of Airway Resistance by the Interrupter Technique A third method to noninvasively measure airway resistance, used primarily in children, is the interrupter technique.
Comparing sR aw , FOT, and R int There are limited studies directly comparing the above indices, and by their nature, appear mainly in children. View this table: View inline View popup Download powerpoint. Table 1. Summary Spirometry remains the gold standard pulmonary function test for determining the presence and severity of air-flow limitation. Discussion Pichurko: I thank Dr Kaminsky for his comments, and his interests certainly overlap with my own. Ruppel: I'd like to follow up on that.
Pichurko: There's a third signal that we use. Kaminsky: We do the same thing. Busse: To go back to your first slide, I don't think what you presented was atypical. Kaminsky: I would agree with you, but in this case the symptoms were very responsive to the inhaler, and I don't know if that was a placebo effect or real. Busse: Right, we don't know what part of the tree they're on: the beginning part of the tree or somewhere else.
Kaminsky: I agree, and that's why some are calling asthma a syndrome as opposed to a disease: because it encompasses facets of different types of symptoms, airway dysfunction, inflammation, and so on. Rundell: Do you do other challenges? Exercise challenge or eucapnic voluntary hyperventilation? Kaminsky: We do exercise challenge with the treadmill, and we only do spirometry during that challenge.
Rundell: Now, have you found that you see the changes in the R aw before you see changes in the FEV 1? Kaminsky: In terms of the methacholine testing?
Kaminsky: It's highly variable. I can't say I've seen a specific pattern that's consistent. Kaminsky: And I mentioned a mechanical ventilator in here, too! Kaminsky: The answer is yes, I think it is worthwhile, and we do that in our practice. Hnatiuk: When you said you use 2 of the 3 measures to stop the bronchoprovocation test, do you deem that positive then?
Kaminsky: Yes. Enright: Do you then take the response to albuterol the ability to quickly reverse the bronchospasm into account when interpreting the results? Kaminsky: I take it into consideration, but it's not the primary thing we look at.
Salzman: I'm not sure I was hearing the 2 of you correctly about this. Kaminsky: No, I won't call the test positive with just subjective end points. Pichurko: Similarly, I would require exceeding the diagnostic threshold for at least one of those objective measures before concluding the provocation study.
Coates: Didn't we talk this morning about the idea that the methacholine challenge test was a good test to rule out asthma? Kaminsky: To me, a negative test is someone who goes up to 16 and flies through it, and there are no changes physiologically, and they have no discomfort. Busse: Well, one could argue the other way. Coates: No disagreement about that, because I am coughing and wheezing even though my PC 20 is greater than Kaminsky: We have these arbitrary cutoffs.
Rundell: One last question. Kaminsky: Yes, and we do the 5 deep breaths method. Rundell: Do you train these patients before you test them, for 6 weeks or so?
E-mail: david. Dr Kaminsky has disclosed relationships with Medical Graphics and Merck. References 1. Optimizing performance of respiratory airflow resistance measurements. Chest ; 6 : — Body plethysmography—its principles and clinical use. Respir Med ; 7 : — OpenUrl PubMed. Lung function in asthma. New York : Lippincott-Raven ; : Tattersfield A , Keeping I. Assessing change in airway calibre - measurement of airway resistance. Brit J Clin Pharm ; 8 4 : — Goldman M.
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Eur Respir J ; 18 3 : — Impulse oscillometry: a measure for airway obstruction. Therefore the resistance to air in the bronchi is greater than the resistance to air in the trachea. The number of airways also plays a large role in the resistance to air, with more airways reducing resistance because there are more paths for the air to flow into.
Therfore, despite the fact that the terminal bronchioles are the smallest airway in terms of radius, their high number compared to the larger airways means that the bronchi actually have greater resistance because there are less of them compared to the terminal bronchioles.
Another important fact is that airway resistance is inversely related to lung volumes because the airways expand a bit as they inflate, so the airways in a fully inflated lung will have lower resistance than a lung after exhalation. Airway resistance can be indirectly measured with body plethysmography, which is an instrument used for measuring changes in volume within a structure, such as the airways. The resistance of the airways is an important indicator of lung health and function and can be used to diagnose lung diseases.
The size of the airways, and thus the resistance can change based on the health and conditions of the lungs. Most lung diseases increase airway resistance in many different ways. For example, in asthma attacks the bronchioles spasm and constrict, which increases resistance.
Emphysema also increases airway resistance because the lung tissue becomes too pliable and it the airways become more difficult to hold open by the flow of air. The air that flows through the lungs varies considerably in the properties of the flow of air. The air flow can either be turbulant, transitional or laminar based on the airway. Laminar flow involves an orderly and concentric distribution of layers of air particles and tends to occur in smaller airways, and has lower resistance.
Turbulent flow is disorganized distribution of the layers of air and tends to occur in larger airways and places where the airways branch, and has a higher resistance. Transitional flow occurs in places that branch within smaller airways, in which the air flow becomes in between laminar and turbulent flow and has moderate resistance.
Laminar and Turbulent Flow : Laminar flow a has orderly layers and low resistance. Turbulent flow b has disorganized layers and high resistance. Learning Objectives Describe airway resistance and how it affects pulmonary ventilation. Key Points Airway resistance is a concept in respiratory physiology that describes the resistance of the respiratory tract to airflow during inspiration and expiration.
Airway resistance can be indirectly measured with body plethysmography. Diseases affecting the respiratory tract can increase airway resistance. Laminar flow is orderly and has low resistance while turbulent flow is disorganized and has high resistance.
Key Terms Airway resistance : Airway Resistance is a concept in respiratory physiology that describes the resistance of the respiratory tract to airflow during inspiration and expiration.
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